Imbalance between 95 kDa type IV collagenase and tissue inhibitor of metalloproteinases in sputum of patients with cystic fibrosis.

Delacourt, Christophe; Bourgeois, Marie; D'Ortho, M. P.; Doit, Catherine; Scheinmann, P.; Navarro, José Luís; Harf, Alain; Hartmann, Daniel; Lafuma, C.

doi:10.1164/ajrccm.152.2.7633740

Cited by 95 publications

(68 citation statements)

References 27 publications

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“…Once secreted, MMP-9 can be activated by many products present in inflammatory airways, especially oxidants (29) and neutrophil elastase (34). In our study, the presence and amount of (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22) Values are medians with 25th-75th percentiles in parentheses; n, no. of neonates.…”

Section: Discussionmentioning

confidence: 75%

“…The 72-and 92-kDa gelatinase activities were characterized by immunoblotting. Supernatants of tracheal aspirates from five infants were pooled and partially purified by using gelatin-Sepharose chromatography, as previously described (11). Samples were separated by SDS-PAGE and were electrophoretically transferred to nitrocellulose.…”

Section: Methodsmentioning

confidence: 99%

“…We also postulated that MMPs may be secreted in excess during the inflammatory response associated with hyaline membrane disease and may, therefore, lead to tissue degradation. Gelatinase B (MMP-9) is the main MMP released by inflammatory cells such as neutrophils and alveolar macrophages (17,35) and has been implicated in human lung diseases such as cystic fibrosis (11) and asthma (22). We thus studied premature infants with hyaline membrane disease to determine whether the profile of gelatinase activities at birth was associated with the subsequent risk of BPD and to examine the possible link between the early postnatal time course of gelatinase activities and clinical outcome.…”

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confidence: 99%

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Gelatinase activities in the airways of premature infants and development of bronchopulmonary dysplasia

Danan

Jarreau

Franco

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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2002.-Matrix-degrading metalloproteinases may play a role in the pathophysiology of bronchopulmonary dysplasia (BDP). We, therefore, evaluated correlations between gelatinase activities [metalloproteinase (MMP)-2 and MMP-9] or tissue inhibitor of metalloproteinase (TIMP)-1 levels present in the airways during the initial phase of hyaline membrane disease and the onset of BPD. Tracheal aspirates were obtained within 6 h of birth (day 0) from 64 intubated neonates with a gestational age Յ30 wk. Forty-five neonates were resampled on day 3 or 5. Total MMP-2 level measured by zymography fell with time, whereas total MMP-9 level and TIMP-1 levels, assayed by ELISA, increased; the MMP-9 increase correlated with the increase in airway inflammatory cell numbers. Among the parameters measured on day 0, 3, or 5, lower total MMP-2 level, lower birth weight, and higher fraction of inspired oxygen on day 0 were significantly and independently associated with the development of BPD. In conclusion, MMP-9 level and TIMP-1 levels increased after birth but are not linked to BPD outcome. In contrast, low MMP-2 level at birth is strongly associated with the development of BPD. metalloproteinase; lung development; newborn; extracellular matrix PREMATURE NEONATES WITH HYALINE membrane disease are at risk of developing bronchopulmonary dysplasia (BPD), as a sequel of both the disease and its treatment. The pathogenesis is unclear, but BPD is thought to result from damage to an immature lung. Mechanical ventilation, oxygen therapy, and airway inflammatory responses have all been implicated in the development of BPD (19). These insults appear to interfere with normal lung maturation, which is incomplete at birth. In particular, they appear to alter alveolar formation, on the basis of morphometric studies of severe BPD (3, 24). Alveolar formation is characterized by the multiplication of alveolar septa and the thinning of interalveolar walls, both of which require intense remodeling of the pulmonary extracellular matrix (4). Changes in matrix turnover have been experimentally linked to abnormal alveolar formation (20). The proteinase-antiproteinase balance in the lung is a key factor in harmonious matrix turnover. In particular, matrix metalloproteinases (MMPs), which can synergistically digest the major macromolecules of connective tissue matrices, have been implicated in physiological regulation of lung growth. The MMP gelatinase A (MMP-2) has been shown to play a role in the major collagen turnover that occurs during early postnatal rat lung growth (1, 2). We postulated that MMP-2 might also participate in human lung development and that inadequate MMP-2 levels in premature lungs exposed to insults could contribute to impaired lung growth and thus to BPD. We also postulated that MMPs may be secreted in excess during the inflammatory response associated with hyaline membrane disease and may, therefore, lead to tissue degradation. Gelatinase B (MMP-9) is the main MMP released by inflammatory cells such as neutrophils and alveolar macroph...

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Section: Discussionmentioning

confidence: 75%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Gelatinase activities in the airways of premature infants and development of bronchopulmonary dysplasia

Danan

Jarreau

Franco

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The expression of these same proteases and antiproteases is critical in tissue repair and remodeling in some pulmonary inflammatory diseases. [5][6][7][8] In allergic asthma, the mechanisms of remodeling of the bronchial tree caused by extracellular matrix deposition are well characterized. Of the MMP family, MMP-9 is the major proteinase that induces bronchial remodeling in asthma.…”

mentioning

confidence: 99%

A murine model of toluene diisocyanate–induced asthma can be treated with matrix metalloproteinase inhibitor

Lee¹,

Song²,

Lee³

et al. 2001

Journal of Allergy and Clinical Immunology

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Background: Toluene diisocyanate (TDI) is a leading cause of occupational asthma. TDI-induced asthma is an inflammatory disease of the airways that is associated with airway remodeling. However, there are little data available on the role of matrix metalloproteinases (MMPs) in TDI-induced asthma. Objective: We evaluated whether MMP-9 participates in the airway inflammation in TDI-induced asthma. An additional aim of the present study was to determine whether MMP inhibitors could be effective therapeutic agents for TDIinduced asthma. Methods: We developed a murine model of TDI-induced asthma to examine the involvement of MMPs by performing 2 sensitizations with 3% TDI and 1 challenge with 1% TDI using ultrasonic nebulization. Toluene diisocyanate (TDI), a low-molecular-weight compound widely used in the production of polyurethane foams, automobile paints, varnishes, and related products, is a leading cause of occupational asthma. 1,2 TDIinduced asthma is characterized by hyperresponsiveness and inflammation of the airways. 2,3 This inflammation is associated with infiltration of lymphocytes, eosinophils, and neutrophils into the bronchial lumen. 3,4 Airway remodeling, which often occurs in the bronchial tree, probably arises as a consequence of inflammatory processes.The extracellular matrix is a dynamic structure, and its homeostasis depends on an equilibrium between synthesis and degradation of extracellular matrix components. A balance between the expression of proteases and antiproteases, particularly the matrix metalloproteinases (MMPs) and their inhibitors, maintains this homeostasis under normal conditions. The expression of these same proteases and antiproteases is critical in tissue repair and remodeling in some pulmonary inflammatory diseases. [5][6][7][8] In allergic asthma, the mechanisms of remodeling of the bronchial tree caused by extracellular matrix deposition are well characterized. Of the MMP family, MMP-9 is the major proteinase that induces bronchial remodeling in asthma. 9,10 In addition, MMP-9 induces the migration of eosinophils and neutrophils across basement membranes. 11,12 Recently, MMPs were reported to play a crucial role in the infiltration of ovalbumin-induced airway inflammatory cells and the induction of airway hyperresponsiveness in a murine model of asthma. 13 However, there are little data available on the role of MMPs in TDIinduced asthma.In the present study we developed a murine model of TDI-induced asthma to examine the involvement of

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“…Accordingly, we hypothesize that another response to apoptotic cells that may be dysregulated in COPD is the production of antiproteases, thereby increasing the protease to antiprotease balance. In keeping with this concept, decreased levels of TIMP are seen in cystic fibrosis (42), together with decreased responses to apoptotic cells (8). Similarly, we are intrigued by the observation that statin treatment can increase the production of TIMPs (9).…”

Section: Antiinflammatory Antiimmunogenic and Antiproteolytic Effecmentioning

confidence: 90%

State of the Art. Apoptosis and Cell Homeostasis in Chronic Obstructive Pulmonary Disease

Henson

Cosgrove²,

Vandivier³

2006

Proceedings of the American Thoracic Society

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Imbalance between 95 kDa type IV collagenase and tissue inhibitor of metalloproteinases in sputum of patients with cystic fibrosis.

Cited by 95 publications

References 27 publications

Gelatinase activities in the airways of premature infants and development of bronchopulmonary dysplasia

Gelatinase activities in the airways of premature infants and development of bronchopulmonary dysplasia

A murine model of toluene diisocyanate–induced asthma can be treated with matrix metalloproteinase inhibitor

State of the Art. Apoptosis and Cell Homeostasis in Chronic Obstructive Pulmonary Disease

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